Nutrient intake and risk of multimorbidity: a prospective cohort study of 25,389 women.

BACKGROUND: Multimorbidity is becoming an increasingly serious public health challenge in the aging population. The impact of nutrients on multimorbidity remains to be determined and was explored using data from a UK cohort study. METHOD: Our research analysis is mainly based on the data collected by the United Kingdom Women's Cohort Study (UKWCS), which recruited 35,372 women aged 35-69 years at baseline (1995 to 1998), aiming to explore potential associations between diet and chronic diseases. Daily intakes of energy and nutrients were estimated using a validated 217-item food frequency questionnaire at recruitment. Multimorbidity was assessed using the Charlson comorbidity index (CCI) through electronic linkages to Hospital Episode Statistics up to March 2019. Cox's proportional hazards models were used to estimate associations between daily intakes of nutrients and risk of multimorbidity. Those associations were also analyzed in multinomial logistic regression as a sensitivity analysis. In addition, a stratified analysis was conducted with age 60 as the cutoff point. RESULTS: Among the 25,389 participants, 7,799 subjects (30.7%) were confirmed with multimorbidity over a median follow-up of 22 years. Compared with the lowest quintile, the highest quintile of daily intakes of energy and protein were associated with 8% and 12% increased risk of multimorbidity respectively (HR 1.08 (95% CI 1.01, 1.16), p-linearity = 0.022 for energy; 1.12 (1.04, 1.21), p-linearity = 0.003 for protein). Higher quintiles of daily intakes of vitamin C and iron had a slightly lowered risk of multimorbidity, compared to the lowest quintile. A significantly higher risk of multimorbidity was found to be linearly associated with higher intake quintiles of vitamin B12 and vitamin D (p-linearity = 0.001 and 0.002, respectively) in Cox models, which became insignificant in multinomial logistic regression. There was some evidence of effect modification by age in intakes of iron and vitamin B1 associated with the risk of multimorbidity (p-interaction = 0.006 and 0.025, respectively). CONCLUSIONS: Our findings highlight a link between nutrient intake and multimorbidity risk. However, there is uncertainty in our results, and more research is needed before definite conclusions can be reached.

Protective Effects of Sesamol on Renal Ischemia-Reperfusion Injury Via Regulation of Nuclear Factor Erythroid 2-Related Factor 2 Pathway.

BACKGROUND: Sesamol is a natural antioxidant known for its potent antioxidant and free radical scavenging properties. This study aimed to explore the therapeutic effects and underlying mechanisms of sesamol in the development of renal ischemia-reperfusion injury (IRI) in mice. METHODS: C57BL/6J wild-type mice were divided into 3 groups: IR group, treated with normal saline after undergoing the IRI procedure; Sesamol + IR group, treated with 30 mg/kg/d of sesamol after the IRI procedure; and Sham group, treated with normal saline but not subjected to the IRI process. Renal IRI was induced by performing a right kidney nephrectomy and subjecting the left kidney to 30-minute ischemia, followed by 24-hour reperfusion. Kidney tissues and serum were collected 24 hours post-IRI to assess the impact of sesamol on renal function after IRI. Serum creatinine and blood urea nitrogen levels were assessed, and renal cell apoptosis was detected through terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. The levels of interleukin 1ß and interleukin 18 in kidney tissues, as well as indicators of oxidative stress, were also measured. Furthermore, Nrf2-deficient mice were used to examine the protective function of the nuclear factor erythroid 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) and NAD(P)H dehydrogenase quinone 1 (NQO1) signaling pathways induced by sesamol, as determined by western blot assay. RESULTS: Sesamol demonstrated significant improvement in renal function, along with reductions in renal tubular injury, cell necrosis, and apoptosis in mice. It also effectively lowered key inflammatory mediator levels. Sesamol exhibited antioxidant properties by reducing malondialdehyde levels and enhancing superoxide dismutase activities 24 hours after IRI. Western blot assay revealed increased Nrf2, HO-1, and NQO-1 protein levels with sesamol treatment. Notably, Nrf2-deficient mice did not exhibit the beneficial effects of sesamol. CONCLUSIONS: This study demonstrates that sesamol effectively alleviates renal IRI by enhancing antioxidant defenses and reducing inflammation potentially through the Nrf2/HO-1 and NQO1 signaling pathways.

YAP1-activated ZNF131 promotes hepatocellular carcinoma cell proliferation through transcriptional regulation of PAIP1.

Zinc finger protein 131 (ZNF131), a member of BTB-ZF transcription factors, has been previously reported as an oncogene in several human cancers. However, the function and underlying mechanism of ZNF131 in hepatocellular carcinoma (HCC) are still unclear. In our study, the upregulated expression of ZNF131 mRNA was confirmed in HCC tissues by analyzing the TCGA and GEO datasets. The immunohistochemical staining data also revealed the overexpression of ZNF131 protein in HCC samples. High expression of ZNF131 predicted poor overall survival and disease-free survival in HCC patients. ZNF131 knockdown inhibited the proliferation and colony formation and led to G2/M phase arrest of HCC cells, while its overexpression promoted HCC cell proliferation, cell cycle progression and colony formation. Moreover, ZNF131 silencing repressed the growth of HCC cells in nude mice. Yes-associated protein 1 (YAP1) was recognized as an upstream regulator of ZNF131. Both YAP1 knockdown and inactivation reduced ZNF131 expression in HCC cells, and YAP1 overexpression enhanced ZNF131 level. Interestingly, we found that poly(A) binding protein interacting protein 1 (PAIP1) was a novel target of ZNF131. ZNF131 silencing downregulated while ZNF131 overexpression upregulated PAIP1 expression in HCC cells. The luciferase reporter assay demonstrated that ZNF131 regulated PAIP1 expression at the transcription level. Notably, we revealed that ZNF131 activated the AKT signaling by enhancing PAIP1 expression in HCC cells. AKT inhibitor markedly attenuated ZNF131-enhanced HCC cell proliferation. Restoring PAIP1 expression abrogated the inhibitory effects of ZNF131 knockdown on HCC cell proliferation and colony formation. To conclude, ZNF131 was highly expressed and acted as an oncogene in HCC. ZNF131, which was activated by YAP1, promoted HCC cell proliferation through transcriptional regulation of PAIP1.

Symbiotic hemolymph bacteria reduce hexavalent chromium to protect the host from chromium toxicity in Procambarus clarkii.

Hexavalent chromium (Cr(VI)) is a cytotoxic heavy metal pollutant that adversely affects all life forms. Interestingly, the crustacean Procambarus clarkii exhibits a relatively high tolerance to heavy metals. The underlying mechanisms remain unclear. In this study, we investigated the role of symbiotic bacteria in P. clarkii in alleviating Cr(VI)-induced damage and explored their potential mechanisms of action. Through transcriptomic analysis, we observed that Cr(VI) activated P. clarkii's antimicrobial immune responses and altered the bacterial composition in the hemolymph. After antibiotic treatment to reduce bacterial populations, Cr(VI)-induced intestinal and liver damage worsened, and crayfish exhibited lower levels of GSH/CAT/SOD activity. The Exiguobacterium, the symbiotic bacteria in the hemolymph of P. clarkii, were proved to be primary contributor to Cr(VI) tolerance. Further investigation suggested that it resists Cr(VI) through the activation of the ABC transporter system and the reduction of Cr(VI) via the reductase gene nfsA. To validate the role of Exiguobacterium in Cr(VI) tolerance, crayfish treated with antibiotics then supplemented with Exiguobacterium H6 and recombinant E. coli (with the nfsA gene), reduced Cr(VI)-induced ovarian damage. Overall, this study revealed that the symbiotic bacteria Exiguobacterium can absorb and reduce hexavalent chromium, mitigating Cr(VI)-induced damage in P. clarkii. These findings provide new insights into hexavalent chromium tolerance mechanisms in crustaceans.

Covid-19 omicron variant infection in neonates of Guangdong province-a report of 52 cases.

Objective: To analyze the clinical characteristics of neonatal infection during the outbreak of COVID-19 omicron variant in Guangdong province of China. Method: The clinical data of neonates infected with COVID-19 omicron variant were collected from three hospitals of Guangdong province, their epidemiological history, clinical manifestation and prognosis were summarized. Results: From December 12, 2022 to January 15, 2023, a total of 52 neonates with COVID-19 infection were identified across three hospitals in Guangdong Province, including 34 males and 18 females. The age of diagnosis was 18.42 ± 6.32 days. 24 cases had clear contact history with adults who were suspected to be infected with COVID-19. The most common clinical manifestation was fever (43/52, 82.7%), the duration of fever was 1-8 days. The other clinical manifestations were cough (27/52, 51.9%), rales (21/52, 40.4%), nasal congestion (10/52, 19.2%), shortness of breath (2/52, 3.8%), and vomiting (4/52, 7.7%). C-reactive protein was only increased in 3 cases. Chest radiological examination was performed in 42 neonates, twenty-three cases showed abnormal chest radiographic findings, including ground-glass opacity and consolidation. Fifty cases were admitted with COVID-19 presentation, two cases were admitted for jaundice. The hospital stay was 6.59 ± 2.77 days. The clinical classification included 3 cases of severe COVID-19 and one critical case. Fifty-one cases were cured and discharged after general treatment, and one critical case with respiratory failure was intubated and transferred to another hospital. Conclusion: The COVID-19 omicron variant infection in neonates is usually mild. The clinical manifestation and laboratory results are not specific, and the short-term prognosis is good.

Effect of Early versus Delayed Use of Norepinephrine on Short-Term Outcomes in Patients with Traumatic Hemorrhagic Shock: A Propensity Score Matching Analysis.

Background: Guidelines recommend norepinephrine (NE) for the treatment of fatal hypotension caused by trauma. However, the optimal timing of treatment remains unclear. Objective: We aimed to investigate the effect of early versus delayed use of NE on survival in patients with traumatic haemorrhagic shock (HS). Materials and Methods: From March 2017 to April 2021, 356 patients with HS in the Department of Emergency Intensive Care Medicine of the Affiliated Hospital of Yangzhou University were identified using the emergency information system and inpatient electronic medical records for inclusion in the study. Our study endpoint was 24 h mortality. We used a propensity score matching (PSM) analysis to reduce bias between groups. Survival models were used to evaluate the relationship between early NE and 24 h survival. Results: After PSM, 308 patients were divided equally into an early NE (eNE) group and a delayed NE (dNE) group. Patients in the eNE group had lower 24 h mortality rates than those in the dNE group (29.9% versus 44.8%, respectively). A receiver operating characteristic analysis demonstrated that a cut-off point for NE use of 4.4 h yielded optimal predictive value for 24 h mortality, with a sensitivity of 95.52%, a specificity of 81.33% and an area under the curve value of 0.9272. Univariate and multivariate survival analyses showed that the survival rate of patients in the eNE group was higher (p < 0.01) than those in the dNE group. Conclusion: The use of NE within the first 3 h was associated with a higher 24 h survival rate. The use of eNE appears to be a safe intervention that benefits patients with traumatic HS.

The emerging role of exosomes in the development of testicular.

The mechanisms of testicular development in mammals are complex. Testis is an organ that produces sperm and secretes androgens. It is rich in exosomes and cytokines that mediate signal transduction between tubule germ cells and distal cells, promoting testicular development and spermatogenesis. Exosomes are nanoscale extracellular vesicles that transmit information between cells. By transmitting information, exosomes play an important role in male infertility diseases such as azoospermia, varicocele, and testicular torsion. However, due to the wide range of sources of exosomes, extraction methods are numerous and complex. Therefore, there are many difficulties in studying the mechanisms of exosomal effects on normal development and male infertility. Therefore, in this review, first, we introduce the formation of exosomes and methods for culturing testis and sperm. Then, we introduce the effects of exosomes on different stages of testicular development. Finally, we summarize the prospects and shortcomings of exosomes when used in clinical applications. We lay the theoretical foundation for the mechanism of the influence of exosomes on normal development and male infertility.

The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a dominant cause of death and disability worldwide. A sharp increase in intracranial pressure after SAH leads to a reduction in cerebral perfusion and insufficient blood supply for neurons, which subsequently promotes a series of pathophysiological responses leading to neuronal death. Many previous experimental studies have reported that excitotoxicity, mitochondrial death pathways, the release of free radicals, protein misfolding, apoptosis, necrosis, autophagy, and inflammation are involved solely or in combination in this disorder. Among them, irreversible neuronal apoptosis plays a key role in both short- and long-term prognoses after SAH. Neuronal apoptosis occurs through multiple pathways including extrinsic, mitochondrial, endoplasmic reticulum, p53 and oxidative stress. Meanwhile, a large number of blood contents enter the subarachnoid space after SAH, and the secondary metabolites, including oxygenated hemoglobin and heme, further aggravate the destruction of the blood-brain barrier and vasogenic and cytotoxic brain edema, causing early brain injury and delayed cerebral ischemia, and ultimately increasing neuronal apoptosis. Even there is no clear and effective therapeutic strategy for SAH thus far, but by understanding apoptosis, we might excavate new ideas and approaches, as targeting the upstream and downstream molecules of apoptosis-related pathways shows promise in the treatment of SAH. In this review, we summarize the existing evidence on molecules and related drugs or molecules involved in the apoptotic pathway after SAH, which provides a possible target or new strategy for the treatment of SAH.

Effects of early cognitive rehabilitation training on cognitive function and quality of life in critically ill patients with cognitive impairment: A randomised controlled trial.

BACKGROUND: Patients often develop cognitive dysfunction during admission to the ICU and after being transferred out of the ICU, which leads to physical disorders, sleep disorders, and psychological stress.Cognitive rehabilitation training can significantly improve patients' planning, decision-making ability, and executive function. OBJECTIVE: The aim of this study was to explore the role of early cognitive rehabilitation training in improving cognitive impairment in critically ill patients. METHODS: This study was a prospective, randomised, controlled clinical trial conducted from January 2017 to June 2021. Critically ill patients with cognitive impairment admitted to the Department of Intensive Care Medicine of The Third Hospital of Mianyang were randomly divided into the control (n = 68) and intervention groups (n = 68). Cognitive rehabilitation training (including digital operating system training, music therapy, aerobic training, and mental health intervention) was applied to the patients in the intervention group for 6 months, while the control group did not receive any cognitive intervention. Before 3 and 6 months after enrolment, the Montreal Cognitive Assessment and the 36-Item Short Form Health Survey Scale were used to evaluate cognitive function and quality of life, respectively, in both groups. RESULTS: A total of 136 critical patients were included in the final analysis. There were no significant differences in sex, age, years of education, complications, intensive care unit hospitalisation time, mechanical ventilation time, or the total score of the Montreal Cognitive Assessment scale when transferred out of the intensive care unit in 24 hours between the two groups. Six months later, the results of the follow-up showed that the cognitive function score in the intervention group was significantly higher than that in the control group (26.69 ± 2.49 vs. 23.03 ± 3.79). The analysis of quality of life showed that the scores in all areas in the intervention group improved. There were significant differences in physical functioning (69.02 ± 8.14 vs. 63.38 ± 11.94), role physical (62.02 ± 12.18 vs. 58.09 ± 8.83), general health (46.00 ± 15.21 vs. 40.38 ± 13.77), vitality (61.00 ± 11.01 vs. 54.38 ± 13.80), social functioning (70.00 ± 10.29 vs. 64.41 ± 13.61), role emotional (78.00 ± 8.00 vs. 72.15 ± 12.18), and mental health (71.00 ± 12.33 vs. 55.37 ± 10.76) between the two groups (P < 0.05). CONCLUSION: Early cognitive rehabilitation training can improve cognitive impairment in critically ill patients and their quality of life.

Experimental Study on the Inhibitory Effect of Eugenol on Inflammatory Activation of Hepatic Stellate Cells by MSCs / 中山大学学报(医学科学版)

ObjectiveThis study aimed to investigate the effects of eugenol on inhibiting the inflammatory activation of human umbilical cord mesenchymal stem cells （HUC-MSCs） and the pro-inflammatory phenotype of hepatic stellate cells （HSCs） in liver fibrosis， and to explore their underlying mechanisms. MethodsHUC-MSCs were cultured and identified in vitro， and the toxicity of eugenol to HUC-MSCs was evaluated by MTT method. The effect of eugenol on the migration ability of HUC-MSCs was investigated by in vitro scratch test. The expression of α-SMA， COL1A1， Smad2/3 and p-Smad2/3 of LX-2 cells activated by TGF-β1 treated with EU-MSCs-CM and MSCs-CM were detected by WB assay. EU-MSCs-CM and MSCs-CM treated THP-1 macrophages stimulated with Lipopolysaccharide （LPS） were analyzed for the expression of surface markers CD11b， CD86， and CD206 by flow cytometry. Additionally， the expression of pro-inflammatory genes TNF-α， IL-1β， and IL-6 in THP-1 macrophages was detected by qPCR. ResultsThe results of MTT method showed that the viability of the cells remained above 90% after 24 h and 48 h treatment at 0， 7.5， 15 μg/mL. In vitro scratches showed that eugenol treatment enhanced HUC-MSCs migration. WB results showed that compared with MSCs-CM treatment， EU-MSCs-CM treatment significantly inhibited the expression of α-SMA， COL1A1， Smad2/3， and p-Smad2/3 of activated HSCs. Flow cytometry showed that compared with MSCs-CM treatment， EU-MSCs-CM treatment had a more significant inhibitory effect on CD86， a M1-type polarization marker in THP-1 macrophages. The results of qPCR experiment showed that compared with MSCs-CM treatment， EU-MSCs-CM treatment more significantly inhibited the expressions of TNF-α， IL-1β and IL-6 of THP-1 macrophage proinflammatory genes. ConclusionsEugenol enhances the inhibitory effect of HUC-MSCs on inflammatory activation of HSCs， possibly by regulating TGF-β1/Smads signaling pathway. It also enhances the inhibitory effect of HUC-MSCs on the pro-inflammatory phenotype of macrophages. Proinflammatory macrophages can promote inflammatory activation of HSCs.

Prediction of factors influencing the timing and prognosis of early tracheostomy in patients with multiple rib fractures: A propensity score matching analysis.

Objective: To investigate the factors affecting the timing and prognosis of early tracheostomy in multiple rib fracture patients. Methods: A retrospective case-control study was used to analyze the clinical data of 222 patients with multiple rib fractures who underwent tracheotomy in the Affiliated Hospital of Yangzhou University from February 2015 to October 2021. According to the time from tracheal intubation to tracheostomy after admission, the patients were divided into two groups: the early tracheostomy group (within 7 days after tracheal intubation, ET) and late tracheostomy group (after the 7th day, LT). Propensity score matching (PSM) was used to eliminate the differences in baseline characteristics Logistic regression was used to predict the independent risk factors for early tracheostomy. Kaplan-Meier and Cox survival analyses were used to analyze the influencing factors of the 28-day survival. Results: According to the propensity score matching analysis, a total of 174 patients were finally included in the study. Among them, there were 87 patients in the ET group and 87 patients in the LT group. After propensity score matching, Number of total rib fractures (NTRF) (P < 0.001), Acute respiratory distress syndrome (ARDS) (P < 0.001) and Volume of pulmonary contusion(VPC) (P < 0.000) in the ET group were higher than those in the LT group. Univariate analysis showed that the patients who underwent ET had a higher survival rate than those who underwent LT (P = 0.021). Pearson's analysis showed that there was a significant correlation between NTRF and VPC (r = 0.369, P = 0.001). A receiver operating characteristic(ROC)curve analysis showed that the areas under the curves were 0.832 and 0.804. The best cutoff-value values of the VPC and NTRF were 23.9 and 8.5, respectively. The Cox survival analysis showed that the timing of tracheostomy (HR = 2.51 95% CI, 1.12-5.57, P = 0.004) and age (HR = 1.53 95% CI, 1.00-2.05, P = 0.042) of the patients had a significant impact on the 28-day survival of patients with multiple rib fractures. In addition, The Kaplan-Meier survival analysis showed that the 28-day survival of patients in the ET group was significantly better than that of the LT group, P = 0.01. Conclusions: NTRF, ADRS and VPC are independent risk factors for the timing and prognosis of early tracheotomy. A VPC ≥ 23.9% and/or an NTRF ≥ 8.5 could be used as predictors of ET in patients with multiple rib fractures. Predicting the timing of early tracheostomy also need prediction models in the future.

Bioinformatics Analysis Screened and Identified Key Genes as Potential Biomarkers for Progression of Lung Cancer.

OBJECTIVE: To screen and identify key genes as potential biomarkers of lung cancer using bioinformatics analysis. STUDY DESIGN: Observational study. PLACE AND DURATION OF STUDY: Department of Critical Care Medicine, the First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China, from August 2018 to April 2021. METHODOLOGY: Independent microarray datasets (GSE85841 and GSE118370) were downloaded from the Gene Expression Omnibus (GEO) database and the differentially expressed genes (DEGs) were screened using GEO2R. Cytohubba was employed to identify the hub genes. Cellular component analysis, hierarchical clustering, and survival analyses of hub genes were performed via BiNGO, UCSC, and cBioPorta. A series of analyses of FGF2 and PIK3R1 were conducted using Oncomine. RESULTS: A total of 463 DEGs were identified and 11 hub genes were determined. BDNF, FGF2, JAK2, NCAM1, CAV1, TJP1, and PIK3R1 may affect the survival probability and life expectancy of lung cancer patients, but the p-values were not statistically significant. FGF2 and PIK3R1 had the highest node degrees, 40 and 32 respectively. The expression of FGF2 and PIK3R1 were significantly lower in the 4 lung cancer data sets compared with non-lung cancer tissues. And the low expression of FGF2 and PIK3R1 is related to tumor grades, family history of cancer, multiple tumors present, and prior therapy of lung cancer. CONCLUSION: Evaluation of FGF2 and PIK3R1 as potential biomarkers can contribute to the subsequent theoretical analysis of potential molecular mechanisms and development of lung cancer, so that the diagnosis of lung cancer may be more accurate, and it is possible to provide therapeutic and prognostic medicine targets. KEY WORDS: Lung neoplasms, Differentially expressed genes, Bioinformatical analysis, Microarray analysis, biomarkers.

Identification and validation of redox-immune based prognostic signature for hepatocellular carcinoma.

The intimate interaction between redox signaling and immunity has been widely revealed. However, the clinical application of relevant therapeutic is unavailable due to the absence of validated markers that stratify patients. Here, we identified novel biomarkers for prognosis prediction in hepatocellular carcinoma (HCC). Prognostic redox-immune-related genes for predicting overall survival (OS) of HCC were identified using datasets from TCGA, LIRI-JP, and GSE14520. LASSO Cox regression was employed to construct the signature model and generate a risk score in the TCGA cohort. The signature contained CDO1, G6PD, LDHA, GPD1L, PPARG, FABP4, CCL20, SPP1, RORC, HDAC1, STC2, HDGF, EPO, and IL18RAP. Patients in the high-risk group had a poor prognosis compared to the low-risk group. Univariate and multivariate Cox regressions identified this signature as an independent factor for predicting OS. Nomogram constructed by multiple clinical parameters showed good performance for predicting OS indicated by the c-index, the calibration curve, and AUC. GSEA showed that oxidoreductase activity and peroxisome-related metabolic pathways were enriched in the low-risk group, while glycolysis activity and hypoxia were higher in the high-risk group. Furthermore, immune profiles analysis showed that the immune score and stromal score were significantly decreased in the high-risk group in the TCGA cohort. There was a considerably lower infiltration of anti-tumor immune cells while a higher proportion of pro-tumor immune cells in silico. Immune markers were distinctly expressed between the subgroups, and redox-sensitive immunoregulatory biomarkers were at higher levels in the high-risk group. Altogether, we identified a redox-immune prognostic signature. A more severe redox perturbation-driven immunosuppressive environment in the high-risk group stratified by the signature may account for poor survival. This may provide a clue to the combined therapy targeting redox and immune in HCC.

Renewable lignin-based surfactant modified layered double hydroxide and its application in polypropylene as flame retardant and smoke suppression.

A novel and environmentally friendly lignin-based surfactant sodium lignosulfonate (SLS) modified layered double hydroxide (LDH) flame retardant (LDH-LS) was fabricated via co-precipitation method, and subsequently incorporated into polypropylene (PP) matrix to obtain the PP and LDH-LS composites (PP/LDH-LS) by melt blending method. The XRD, FT-IR and XPS results indicated that SLS had successfully modified LDH by adsorbing on the surface of the LDH nanosheet. The WCA and SEM results revealed that the hydrophobic property of LDH-LS had been evidently improved, and it displayed a more homogeneous dispersion than virgin LDH in the PP matrix. Furthermore, cone calorimetry tests (CCT) illustrated that the peak heat release rate (PHRR), total heat release (THR), and total smoke release (TSR) of PP/LDH-LS composites exhibited declines of 62.9%, 25.1%, and 43.3% compared with those of Neat PP, respectively. Besides, the PP/LDH-LS achieved a LOI value of 29.4% and a UL-94 V-0 rating, whereas the PP/LDH showed only a LOI value of 25.2% and a UL-94 V-2 rating at 20 wt% loading. These improvements of flame retardant properties can be attributed to that the well-dispersed LDH-LS and synergistic flame retardancy between LDH and SLS.

Comparison of the gut microbiota of short-term and long-term medical workers and non-medical controls: a cross-sectional analysis.

OBJECTIVES: The hospital environment has been implicated in the enrichment and exchange of pathogens and antibiotic resistance, but its potential in shaping the symbiotic microbial community of hospital staff is unclear. This study was designed to evaluate the alteration of the gut microbiome in medical workers compared to non-medical controls. METHODS: A prospective cross-sectional cohort study was conducted in the intensive care unit (ICU) and other departments of a centre in north-eastern China. Faecal samples of 175 healthy medical workers-short-term (1-3 months) workers (n = 80) and long-term (>1 year) workers (n = 95)-and 80 healthy non-medical controls were analysed using 16S rRNA amplicon sequencing. The hospital environmental samples (n = 9) were also analysed. RESULTS: The gut microbiomes of medical workers exhibited marked deviations in diversity and alteration in microbial composition and function. Short-term workers showed significantly higher abundances of taxa such as Lactobacillus, Butyrivibrio, Clostridiaceae, Clostridium, Ruminococcus, Dialister, Bifidobacterium, Odoribacter, and Desulfovibrio and lower abundances of Bacteroides and Blautia than the controls. Long-term workers showed higher abundances of taxa such as Dialister, Veillonella, Clostridiaceae, Clostridium, Bilophila, Desulfovibrio, Pseudomonas, and Akkermansia and lower abundances of Bacteroides and Coprococcus than the controls. The medical workers' department (ICU versus non-ICU) and position (resident doctor versus nursing staff) also impacted their gut microbiome. Compared with the non-ICU workers, workers in the ICU showed a significant increase in the abundances of Dialister, Enterobacteriaceae, Phascolarctobacterium, Pseudomonas, Veillonella, and Streptococcus and a marked depletion of Faecalibacterium, Blautia, and Coprococcus. In contrast with the nursing staff, the resident doctors showed a significant increase in Erysipelotrichaceae and Clostridium and a decrease in Bacteroides, Blautia, and Ruminococcus in the gut microbiome. Moreover, we found that the microbiota of hospital environments potentially correlated with the workers' gut microbiota. CONCLUSIONS: Our findings demonstrated structural changes in the gut microbial community of medical workers.

A Comparative Analysis of Methods for Titering Reovirus.

BACKGROUND: A key challenge in the process of virus amplification is the need for a simple and convenient method for measuring virus titers. OBJECTIVE: Real-time unlabeled cell analysis (RTCA) was used to establish a standard curve of correlation between half-cell index time (CIT50) and virus titer. At the same time, the virus titer from tunable resistance pulse detection (TRPS) technology was compared with the traditional median tissue culture infectious dose (TCID50) method to evaluate the feasibility and application value of the RTCA technique and TRPS technology. METHODS: Cell index (CI) values for L929 cells under different culture conditions were detected, and the appropriate initial cell inoculation density was screened. The half-cell index (CI50) values of reovirus infected L929 cells with TCID50 titers were analyzed by RTCA, the CI50-TCID50 standard curve was created, and a regression equation was developed. RTCA, TCID50, and TRPS methods were used to detect the reovirus titer obtained by the amplification, and the sensitivity and feasibility of the CIT50-TCID50 standard curve method were analyzed. The virus titer was detected by TRPS technology and the TCID50 method. RESULTS: L929 cells were best propagated at an initial density of 6 × 103 cells/well. After infecting L929 cells with different titers of reference reovirus, the linear correlation of CIT50 and TCID50 was y = -2.1806x + 71.023 (R2 = 0.9742). The titer resulting from the RTCA assay was 7×109.6821 pfu/mL, from the TRPS assay was 4.52×1010 pfu/mL, and from the TCID50 assay was 7×109.467 pfu/mL. CONCLUSION: The CIT50-TCID50 standard curve method established by the RTCA technique can be used to quantitatively detect reovirus titer with L929 cells. Compared with the TCID50 method, it takes a relatively short time and has high sensitivity and accuracy. The TRPS technology requires even less time to quantify the virus, but its precision is lower than that of the TCID50 method and RTCA technology. This study provides new technical methods for assessing the virulence of infectious live reovirus particles. Lay Summary: After amplification of the virus, we need to detect the virus titers (the virulence of the virus). The traditional method is to use the virus to infect cells, and then the virus titers can be calculated by 50% of the cells infected. However, this traditional method is time consuming. The ways of RTCA (a real-time cell analysis technique) and TRPS (a nano-bioparticle analysis technique) help us to detect viral titers. The consistency of these three methods determines their feasibility and accuracy. If they are feasible, then these two simple technologies will provide new ideas for detecting viral titers.

Fabrication of green alginate-based and layered double hydroxides flame retardant for enhancing the fire retardancy properties of polypropylene.

An efficient and bio-based alginate pillared hydrotalcite (SA@LDHs) was fabricated via calcination-reconstruction manner with sodium alginate (SA) and hydrotalcite (LDHs-C), and used as novel flame retardant for polypropylene (PP). The morphologies and combustion properties of SA@LDHs and its hybrid with PP composites (PP/SA@LDHs) had been characterized by SEM, TGA, cone calorimetry, LOI and UL-94 measurements. With 30 wt% loading, the SA@LDHs achieved a LOI value of 30.9 % and a UL-94 V-0 rating, whereas the LDHs-C exhibited only LOI value of 27.6 % and a UL-94 V-1 rating. The peak heat release rate, total heat release and total smoke production of PP/SA@LDHs were 260.8 kW m-2, 61.3 MJ m-2 and 8.2 m2, respectively, which presented declines of 69.2 %, 42.8 % and 32.2 % compared with those of Neat PP. These improvements could be attributed to the presence of the radical-trapping effect of SA, which leading to promote PP chains to participate in the carbonization process.

MicroRNA-769-5p contributes to the proliferation, migration and invasion of hepatocellular carcinoma cells by attenuating RYBP.

Hepatocellular carcinoma (HCC) is the commonest primary liver cancer with highly aggressive features. MicroRNAs (miRNAs) are demonstrated to play important roles in the tumorigenesis and progression of HCC. miR-769-5p is a recently identified cancer-associated miRNA. But, the expression level of miR-769-5p and its function in HCC are unexplored. In this study, we found that miR-769-5p expression was obviously increased in HCC samples compared to adjacent noncancerous liver tissues. Additionally, we revealed that miR-769-5p was over-expressed in HCC cells as compared with LO2 cells. Notably, HCC tissues from patients with tumor size ≥5 cm, venous infiltration and advanced tumor stages showed higher levels of miR-769-5p compared to those from corresponding controls. Interestingly, our data indicated that HCC patients highly expressing miR-769-5p had significant shorter survivals. Next, functional experiments verified that miR-769-5p knockdown markedly suppressed HCC cell proliferation, migration and invasion. Conversely, ectopic expression of miR-769-5p promoted these biological behaviors of Hep3B cells. Furthermore, depletion of miR-769-5p repressed the growth and metastasis of HCCLM3 cells in vivo. Importantly, miR-769-5p inversely modulated RING1 and YY1 binding protein (RYBP) by directly binding to 3' untranslated region (UTR) in HCC cells. The expression of RYBP mRNA was down-regulated in HCC tissues and negatively correlated with miR-769-5p level. RYBP overexpression remarkably inhibited the proliferation, migration and invasion of HCCLM3 cells. Accordingly, knockdown of RYBP partially abolished miR-769-5p silencing-induced tumor suppressive effects on HCCLM3 cells. In summary, our study revealed the up-regulated expression of miR-769-5p, which contributed to HCC progression possibly by targeting RYBP.

[Fabrication of the Heterojunction Photocatalyst MoS2/BiOI and Its Investigation of Its Photocatalytic Reduction and Oxidation Activities].

Based on a two-step approach, a flower-like MoS2/BiOI composite with a heterojunction has been successfully fabricated. X-ray diffraction (XRD), scanning electron microscopy (SEM), UV-Vis diffuse reflectance spectroscopy (DRS), and X-ray photoelectron spectroscopy (XPS) were used to characterize the prepared MoS2/BiOI. The formation mechanism of this heterostructure was investigated. The valence band (VB) and conduction band (CB) of the MoS2/BiOI heterojunction have been calculated based on electrochemical characterization, implying the formation of a type I band alignment. The photodegradation of Rhodamine B (RhB) and Cr6+ were used to assess photocatalytic reduction and oxidation activities. The results show that the MoS2/BiOI composite structures perform much better than pristine MoS2 and BiOI. Among the composites with various MoS2 contents, 2% MoS2/BiOI exhibits the best efficiency with respect to the degradation of RhB. After irradiation for 20 minutes, the degradation rate of RhB was 98.82%, which is 1.79 times higher than that using pure BiOI. After irradiation for 80 minutes, the removal of Cr6+ was 97.87%, which is 3.85 times higher than that using pure BiOI. Holes and·O2- are the main reactive species during the photocatalytic process of RhB degradation; holes play the leading role.